title: Vitamin D deficiency in undifferentiated connective tissue disease.
abstract: BACKGROUND
  Both experimental and clinical data provide evidence that vitamin D is one of those important environmental factors that can increase the prevalence of certain autoimmune diseases such as systemic lupus erythematosus, rheumatoid arthritis, insulin-dependent diabetes mellitus, and inflammatory bowel disease. The aim of the present study was to investigate the prevalence of vitamin D insufficiency in patients with undifferentiated connective tissue disease (UCTD).
  
  
  METHODS
  Plasma 25(OH)D3 levels in 161 UCTD patients were measured in both summer and winter periods. Autoantibody profiles (antinuclear antibody, anti-U1-ribonucleoprotein, anti-SSA, anti-SSB, anti-Jo1, anti-Scl70, anti-double-stranded DNA, anti-centromere, anti-cardiolipin, rheumatoid factor, and anti-cyclic citrullinated peptide) and clinical symptoms of the patients were assessed.
  
  
  RESULTS
  Plasma levels of 25(OH)D3 in UCTD patients were significantly lower compared with controls in both summer and winter periods (UCTD summer: 33 +/- 13.4 ng/mL versus control: 39.9 +/- 11.7 ng/mL, P = 0.01; UCTD winter: 27.8 +/- 12.48 ng/mL versus control: 37.8 +/- 12.3 ng/mL, P = 0.0001). The presence of dermatological symptoms (photosensitivity, erythema, and chronic discoid rash) and pleuritis was associated with low levels of vitamin D. During the average follow-up period of 2.3 years, 35 out of 161 patients (21.7%) with UCTD further developed into well-established connective tissue disease (CTD). Patients who progressed into CTDs had lower vitamin D levels than those who remained in the UCTD stage (vitamin D levels: CTD: 14.7 +/- 6.45 ng/mL versus UCTD: 33.0 +/- 13.4 ng/mL, P = 0.0001).
  
  
  CONCLUSIONS
  In patients with UCTD, a seasonal variance in levels of 25(OH)D3 was identified and showed that these levels were significantly lower than in controls during the corresponding seasons. Our results suggest that vitamin D deficiency in UCTD patients may play a role in the subsequent progression into well-defined CTDs.
authors.affiliation: Division of Clinical Immunology, 3rd Department of Medicine, Medical and Health Science Center, University of Debrecen, Moricz Zs, Str, 22, Debrecen, 4032, Hungary. zold_eva@yahoo.com
authors.forename: Eva
authors.initials: E
authors.lastname: Zold
authors.forename: Peter
authors.initials: P
authors.lastname: Szodoray
authors.forename: Janos
authors.initials: J
authors.lastname: Gaal
authors.forename: János
authors.initials: J
authors.lastname: Kappelmayer
authors.forename: Laszlo
authors.initials: L
authors.lastname: Csathy
authors.forename: Edit
authors.initials: E
authors.lastname: Gyimesi
authors.forename: Margit
authors.initials: M
authors.lastname: Zeher
authors.forename: Gyula
authors.initials: G
authors.lastname: Szegedi
authors.forename: Edit
authors.initials: E
authors.lastname: Bodolay
mesh_terms: D000328:Adult; D001323:Autoantibodies / Q000097:blood; D002112:Calcifediol / Q000097:blood / Q000172:deficiency*; D002851:Chromatography, High Pressure Liquid; D018450:Disease Progression; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D008947:Mixed Connective Tissue Disease / Q000097:blood* / Q000150:complications* / Q000473:pathology; D015995:Prevalence; D012621:Seasons; D014808:Vitamin D Deficiency / Q000150:complications* / Q000453:epidemiology*
chemical_list: D001323:Autoantibodies; D002112:Calcifediol